The hypothalamic-pituitary axis has an important role in regulating the menstrual cycle. GnRH, a decapeptide produced in the hypothalamus and released in a pulsatile manner, controls the secretion of LH and FSH through a portal vascular system (see Chapter 32). Blockade of the portal system reduces the secretion of LH and FSH and leads to ovarian atrophy and a reduction in ovarian hormone secretion. The secretion of GnRH by the hypothalamus is regulated by neurons from other brain regions. Neurotransmit-ters, such as epinephrine and norepinephrine, stimulate the secretion of GnRH, whereas dopamine and serotonin inhibit secretion of GnRH. In addition, ovarian steroids and peptides and hypothalamic neuropeptides can regulate the secretion of GnRH. GnRH stimulates the pituitary gonadotrophs to secrete LH and FSH. GnRH binds to high-affinity receptors on the gonadotrophs and stimulates the secretion of LH and FSH through a phosphoinositide-pro-tein kinase C-mediated pathway (see Chapter 1).
A graph of LH release throughout the female life span is shown in Figure 38.2. During the neonatal period, LH is released at low and steady rates without pulsatility,- this period coincides with lack of development of mature ovarian follicles and very low to no ovarian estradiol secretion. Pulsatile release begins with the onset of puberty and for several years is expressed only during sleep, this period coincides with increased but asynchronous follicular development and with increased secretion of ovarian estra-diol. Upon the establishment of regular functional menstrual cycles associated with regular ovulation, LH pulsatil-ity prevails throughout the 24-hour period, changing in a monthly cyclic manner. In postmenopausal women whose ovaries lack sustained follicular development and exhibit
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